EPA/600/8-88/013
July, 1987
HEALTH EFFECTS ASSESSMENT
FOR ACROLEIN
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
CINCINNATI, OH 45268
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DISCLAIMER
*
This document has been reviewed 1n accordance with the U.S.
Environmental Protection Agency's peer and administrative review policies
and approved for publication. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
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PREFACE
•
This, report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with acroleln.
All estimates of acceptable Intakes and carcinogenic potency presented In
this document should be considered as preliminary reflecting limited re-
sources allocated to this project. Pertinent toxlcologlc and environmental
data were located through on line literature searches of the TOXLINE and the
CHEMFATE/DATALOG data bases. The basic literature searched supporting this
document Is current up to May, 1986. Secondary sources of Information have
also been relied upon In the preparation of this report and represent large
scale health assessment efforts that entail extensive peer and Agency
review. The following Office of Health and Environmental Assessment (OHEA)
sources have been extensively utilized:
U.S. EPA. 1980a. Ambient Water Quality Criteria for Acrolelns.
Prepared by the Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH for
the Office of Water Regulations and Standards, Washington, DC. EPA
440/5-80-016. NTIS PB81-117277.
U.S. EPA. 1985a. Health and Environmental Effects Profile for
Acroleln. Prepared by the Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincin-
nati, OH for the Office of Solid Waste and Emergency Response,
Washington, DC.
U.S. EPA. 1986a. Health Assessment Document for Acroleln.
Prepared by the Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Research Triangle
Park, NC for the Office of Air Quality Planning and Standards,
Washington, DC. EPA 600/8-86-OHA.
The Intent In these assessments 1s to suggest acceptable exposure levels
for noncarclnogens and risk cancer potency estimates for carcinogens
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited In
scope tending to generate conservative (I.e., protective) estimates.
Nevertheless, the Interim values presented reflect the relative degree of
hazard or risk associated with exposure to the chemical(s) addressed.
Whenever possible, two categories of values have been estimated for
systemic toxicants (toxicants for which cancer Is not the endpolnt of
concern). The first, RfD$ (formerly AIS) or subchronlc reference dose, Is
an estimate of an exposure level that would .not be expected to cause adverse
effects when exposure occurs during a limited time Interval (I.e., for an
Interval that does not constitute a significant portion of the Hfespan).
This type of exposure estimate has not been extensively used, or rigorously
defined, as previous risk assessment efforts have been primarily directed
towards exposures from toxicants In ambient air or water where lifetime
exposure 1s assumed. Animal data used for RFD$ estimates generally
Include exposures with durations of 30-90 days. Subchronlc human data are
111
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rarely available. Reported exposures are usually from chronic occupational
exposure situations or from reports of acute accidental exposure. These
values are developed for both Inhalation (RfD$j) and oral (RfD$o)
exposures.
The RfO (formerly AIC) Is similar In concept and addresses chronic
exposure. It Is an estimate of an exposure level that would not be expected
to cause adverse effects when exposure occurs for a significant portion of
the Hfespan [see U.S. EPA (1980b) for a discussion of this concept]. The
RfO Is route-specific and estimates acceptable exposure for either oral
(RfDg) or Inhalation (RfDj) with the Implicit assumption that exposure
by other routes Is Insignificant.
Composite scores (CSs) for noncarclnogens have also been calculated
where data permitted. These values are used for Identifying reportable
quantities and the methodology for their development Is explained "in U.S.
EPA (1983).
For compounds for which there Is sufficient evidence of carclnogenlclty
RfD$ and RfD values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980b). Since cancer Is a
process that Is not characterized by a threshold, any exposure contributes
an Increment of risk. For carcinogens, q-|*s have been computed, 1f appro-
priate, based on oral and Inhalation data If available.
1v
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ABSTRACT
In order to place the risk assessment evaluation In proper context,
refer to the preface of this document. The preface outlines limitations
applicable to all documents of this series as well as the appropriate Inter-
pretation and use of the quantitative estimates presented.
The unpublished study by Ujlnsky (n.d.) Indicates that acroleln may be
carcinogenic following oral exposure. Using the significantly Increased
Incidence of adrenal cortical adenomas In female rats found 1n the LlJInksy
(n.d.) study, a human q-|* of 0.17 (mg/kg/day)'1 was derived. Data
Indicating a carcinogenic effect of acroleln following Inhalation exposure
were not available, so an Inhalation q-|* could not be derived.
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ACKNOWLEDGEMENTS
*
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Dr. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and John Helms (Office of
Toxic Substances) was the Project Officer. The final documents In this
series were prepared for the Office of Emergency and Remedial Response,
Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of A1r Quality Planning and Standards
Office of Solid Haste
Office of Toxic Substances
Office of Drinking Water
Editorial review for the document series was provided by the following:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by the
following:
Bette Zwayer, Jacky Bohanon and K1m Davidson
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS
1.
2.
3.
4.
5.
6.
ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1. ORAL
2.2. INHALATION '
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
3.2. CHRONIC
3.2.1. Oral
3.2.2. Inhalation
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS. . . .
3.3.1. Oral
3.3.2. Inhalation
3.4. TOXICANT INTERACTIONS
CARCINOGENICITY
4.1. HUMAN DATA
4.2. BIOASSAYS
4.2.1. Oral
4.2.2. Inhalation
4.3. OTHER RELEVANT DATA
4.4. HEIGHT OF EVIDENCE
REGULATORY STANDARDS AND CRITERIA
RISK ASSESSMENT
6.1. SUBCHRONIC REFERENCE DOSE (RfDs)
6.1.1. Oral (RfOso)
6.1.2. Inhalation (RfDsi)
Paqe
... 1
... 3
... 3
... 3
... 4
... 4
... 4
... 4
. . . 10
. . . 10
. . . 10
, , , 11
. . . 11
. . . 11
. . . 11
. . . 13
. . . 13
. . . 13
. . . 13
13
. . . 14
. . . 16
. . . 18
. . . 20
20
. . . 20
. . . 20
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TABLE OF CONTENTS
6.2. REFERENCE DOSE (RfD)
6.2.1. Oral (Rf00) 20
6.2.2. Inhalation (RfDj) 20
6.3. CARCINOGENIC POTENCY (q^) . . 20
6.3.1. Oral. 20
6.3.2. Inhalation. .... 21
7. REFERENCES 22
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LIST OF ABBREVIATIONS
CAS Chemical Abstract Service
CBI Confidential business Information
CS Composite score
DMSO Dimethyl sulfoxlde
DNA Oeoxyrlbonuclelc acid
1050 Oose lethal to 50% of recipients
LOAEL Lowest-observed-adverse-effect level
MED Minimum effective dose
NOEL No-observed-effect level
PEL Permissible exposure limit
ppm Parts per million
RD5Q Dose at which respiratory rate 1s decreased 50%
RfD Reference dose
RfDj Inhalation reference dose
RfDg Oral reference dose
RfD$ Subchronlc reference dose
Subchronlc Inhalation reference dose
Subchronlc oral reference dose
RV(j Dose-rating value
RVe Effect-rating value
STEL Short-term effect level
TLV Threshold limit value
TWA Time-weighted average
1x
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1. ENVIRONMENTAL CHEMISTRY AND FATE
Selected physical and chemical properties and environmental fate of
acroleln are listed 1n Table 1-1.
Acroleln 'exposed to sunlit atmospheres Is decomposed rapidly by reaction
with photochemically generated hydroxyl radicals (estimated half-lives of
0.23-0.42 days). Products of the reaction of acroleln with OH radical
Include CO, formaldehyde, glycoaldehyde, and, 1n the presence of nitrogen
oxides, peroxynHrates and nitric add. Reaction of acroleln with ozone may
also contribute to the atmospheric depletion of acroleln (estimated half-
life of 2 days). The presence of acroleln In rainwater samples suggests
that wet deposition may contribute to the removal of acroleln from air (U.S.
EPA, 1985a). In aquatic media, acroleln apparently undergoes rapid but
reversible hydratlon to product p-hydroxyprop1onaldehyde. Removal by
blodegradatlon and volatilization may a.lso be significant. Based on water
solubility and the octanol/water partition coefficient, acroleln 1s not
expected to bloaccumulate In aquatic organisms; however, the experimentally
determined maximum bloconcentratlon factor of 344 1n blueglll sunflsh
Indicates potential for moderate bloaccumulatlon (U.S. EPA, 1985a). The
half-life of acroleln In soil systems could not be located 1n the literature
searched. The estimated soil adsorption coefficients of 5 and 32 suggest
that acroleln 1s readily susceptible to leaching (U.S. EPA, 1985a). The
relatively high vapor pressure of acroleln (220 mm Hg at 20°C; 269 mm Ho at
2S°C) suggests that It may volatilize rapidly from dry soil surfaces.
0103h -1- 10/23/86
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TABLE 1-1
Selected Physical and Chemical Properties and Half-Lives for Acroleln
Property
Value
Reference
CAS number:
Chemical class:
Molecular weight:
Vapor pressure:
Water solubility:
Log octanol/water
partition coefficient:
Bloconcentratlon factor
Soil adsorption coefficient:
Half-lives 1n
Air:
Water:
107-02-8
unsaturated aldehyde
56.06
220 mm Hg (20°C)
269 mm Hg (2S°C)
330 mm Hg (30°C)
2.00xlO» to 2.08xlO»
mg/l (20°C)
4.00xlO~» mg/l (25°C)
-0.01
<344, blueglll
Tlepomls macrochlrus)
0.6-0.23 (estimated)
5-32 (estimated)
<1 day (estimated)
<1 day - 3 days
U.S. EPA. 1985a
U.S. EPA, 1985a
Hansch and Leo.
1985
U.S. EPA. 1985a
U.S. EPA, 1985a
U.S. EPA, 1985a
U.S.. EPA, 1985a
0103h
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10/23/86
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
f
2.1. ORAL
Dramlnskl et al. (1983) Indicated that acroleln Is at least partially
absorbed following oral exposure. In this study, the metabolites s-carboxy-
ethylmercapturlc acid or s- (proplonlc acid methyl ester) mercapturlc add
(or both In combination) were detected In the urine of rats orally dosed
with acroleln at 10 mg/kg. The quantity of metabolite recovered was not
reported.
Brabec (1982) stated that the extremely reactive acroleln reacts with
epithelial surfaces, tending to prevent passage of acroleln Into the
Interior of the body. Further Information regarding the absorption of
acroleln following oral exposure could not be located In the available
literature.
2.2. INHALATION
The only study available concerning the absorption of acroleln following
Inhalation exposure was conducted by Egle (1972). In this study, anesthe-
tized mongrel dogs were exposed to acroleln at air concentrations of 0.4-0.6
mg/i (400-600 mg/m3) for 1-3 minutes. Of the Inhaled acroleln, 81-84%
was retained. Egle (1972) also examined retention of acroleln In the upper
respiratory tract In dogs In which the trachea was severed just above the
bifurcation. Only -20% of the Inhaled acroleln reached the lower respira-
tory tract, as retention In the upper tract removed -80% of Inhaled
acroleln. Retention In the lower tract was -70%.
0103h 3- 01/13/87
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. Only limited data concerning the toxic effects of acroleln
following subchronlc oral exposure were available. Albln (1962) (summarized
1n U.S. EPA, 1980a), provided rats with drinking water containing acroleln
at concentrations <200 mg/i for 90 days. The only effect observed was a
slight weight reduction at 200 mg/1 acroleln. This effect was attributed
to the unpalatablllty of the water, which decreased water Intake.
In a similar study by Newell (1958) (reviewed by NAS, 1977), acroleln
was added to drinking water 1n concentrations of 5, 13, 32, 80 and 200
mg/i and given to rats for 90 days. No effects on hematologlcal param-
eters, organ weights or pathology (not otherwise specified) were observed.
The only effect noted was a decrease In water consumption during the first 3
weeks of the study. In a second study (Newell, 1958), male rats were
provided with drinking water containing 600, 1200 or 1800 mg acroleln/i
for 60 days. At 1200 and 1800 mg/l, all rats died from lack of water
Intake. At 600 mg/t, 1/5 rats died. No other effects were reported.
3.1.2. Inhalation. Studies of the toxic effects of subchronlc Inhalation
exposure to acroleln Indicate that Inhalation exposure to acroleln results
In morphological changes 1n the respiratory system, especially the upper
dlrways. A few representative studies conducted at concentrations at or
rear LOAELs will be presented In this section. More complete reviews are
f-vallable In Carson et al. (1981) and Beauchamp et al. (1985).
Lyon et al. (1970) exposed groups of 7 male and 7 female NMRI:0 Sprague-
Oawley rats, similar numbers of Princeton or Hartly guinea pigs, groups of 9
male squirrel monkeys and groups of 2 male beagle dogs to acroleln. The
0103H -4- 10/23/86
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exposure regimens used were acroleln vapor at 0.7 or 3.7 ppm {1.6 or 8.5
mg/m3) for 8 hours/day, 5 days/week for 6 weeks, or continuous exposure
for 90 days at 0.22, 1.0 or 1.8 ppm (0.50, 2.3 or 4.1 mg/m3). Similar
groups of each species were maintained as controls. Body weights and
hematologlcal determinations were recorded before and after exposure.
Immediately before termination of the study, serum alanlne and aspartate
amlnotransferase activities and blood urea nitrogen levels were determined.
Hlstopathologlcal examination of the lungs, heart, liver, spleen and kidneys
was done on all dogs and monkeys and on half of the guinea pigs and rats.
Observation of the exposed animals revealed no signs of toxlclty after
repeated exposures at 0.7 ppm. Hlstologlcal examination of the lungs from
all species exposed repeatedly at 0.7 ppm showed mild chronic Inflammatory
changes and occasional mild emphysema. Inflammatory changes In the bronchi
were more pronounced In monkeys and dogs.
Dogs and monkeys exposed repeatedly to acroleln at 3.7 ppm showed eye
Irritation, excessive salivation and labored breathing. After the first
week of exposure, these signs were less severe, although eye Irritation per-
sisted throughout the study (Lyon et al., 1970). At this exposure regimen,
two monkeys died; both had pulmonary lesions. Rats exposed repeatedly at
3.7 ppm had significantly reduced weight gain. No other signs of toxlclty
were observed In rats or guinea pigs. No effects on hematology or blood
chemistry were observed 1n any species. Nonspecific Inflammatory hlstologlc
changes were found In the lungs, liver and kidneys of all species at 3.7
ppm. Squamous cell metaplasia and basal cell hyperplasla were observed In
the tracheas of dogs and monkeys. Necrotlzlng bronchitis and squamous cell
metaplasia of the lungs were found 1n 7/9 monkeys.
0103h -5- 01/13/87
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Observation of animals exposed at 0.22 ppm continuously for 90 days
revealed no toxic effects. H1stolog1c changes at 0.22 ppm paralleled those
at the 0.7 ppm repeated exposure. In addition, at 0.22 ppm nonspecific
Inflammatory changes were observed In liver, lung, kidney and heart sections
from monkeys, guinea pigs and dogs. Dogs and monkeys exposed continuously
at 1.0 and 1.8 ppm showed severe Irritation as described for the repeated
exposure study. At 1.0 and 1.8 ppm, rats had decreased body weight gains
compared with controls. Guinea pigs exposed continuously at 1.0 ppm showed
pulmonary Inflammation and occasional foci of liver necrosis. At 1.0 ppm,
3/9 rats examined h1stolog1cally had foci of liver necrosis and occasional
pulmonary hemorrhages. Dogs at this exposure level had Inflamed lungs,
liver and kidneys. At 1.8 ppm, all animals examined hlstologlcally showed
Inflammatory changes In the lungs, liver, kidneys, brain and heart. H1sto-
loglcal changes In the lungs and bronchi paralleled those observed after
repeated exposure at 3.7 ppm acroleln (Lyon et al., 1970).
Another study that examined the effects of subchronlc Inhalation expo-
sure to acroleln In several species was conducted by Feron et al. (1978).
Groups of 20 Syrian golden hamsters, 12 SPF Wlstar rats and 4 Dutch rabbits
of each sex were exposed to acroleln vapor at 0, 0.4, 1.4 or 4.9 ppm (0,
0.9. 3.2 or 11.2 mg/m3), 6 hours/day, 5 days/week for 13 weeks. Food
consumption and body weights were measured weekly. Hematology, clinical
chemistry and ur1na!ys1s determinations were made at 12 weeks. At study
termination, necropsies were performed, organ weights were recorded and
hlstopathologlcal examinations of major organs and tissues were performed on
all control and high-dose animals. The respiratory tracts of all animals
were examined hlstopathologlcally.
0103h -6- 10/23/86
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• At 0.4 ppm, no toxic signs were noted In any species. Rabbits were
sneezing and rats and hamsters appeared narcotized at 1.4 ppm. At 4.9 ppm.
Increased salivation and nasal secretion, and eye Irritation were noted In
all species. At the highest dose, 3/12 male and 3/12 female rats died; one
hamster was sacrificed at week 12 when moribund with renal failure.
Decreased weight gain was observed 1n rats and rabbits exposed at 1.4 and
4.9 ppm and In hamsters at 1.4 ppm.
No effects on hematologlcal or clinical chemistry parameters were
observed In any species at any exposure concentration. At 4.9 ppm, relative
weights of lungs In all three species, of the heart and kidneys 1n hamsters
and rats, and of adrenals 1n rats were Increased compared with controls.
At the highest exposure concentration, marked hlstologlc changes were
observed In the epithelium of the nasal cavity of all species. Hyperplasla
1n the trachea was also observed 1n all species at 4.9 ppm, with more severe
hyperplastlc effects 1n rats than In .hamsters or rabbits. H1stolog1cal
changes In the lungs and bronchi (hemorrhage and peMvascular and alveolar
edema) were observed In rats and rabbits exposed at 4.9 ppm. These effects
were not observed In hamsters. At 1.4 ppm acroleln, squamous metaplasia and
neutrophll Infiltration of the nasal mucosa of rats were observed.
As Indicated by the studies of Lyon et al. (1970) and Feron et al.
(1978), rabbits and hamsters seem to be less sensitive to Inhaled acroleln.
Rats seem to be Intermediate In their response to Inhaled acroleln, with
dogs and monkeys being the most sensitive.
A study reported by Costa et al. (1986) and Kutzman et al. (1985)
further Investigated the response of rats to Inhaled acroleln. Groups of
male and female Fischer 344 rats (number unspecified) were exposed to
filtered air 0.4, 1.4 or 4.0 ppm (0.9, 3.2 or 9.2 mg/m3) acroleln for 62
0103h -7- 10/23/86
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days (6 hours/day, 5 days/week). Endpolnts were assessed 6 days after the
final exposure to emphasize the chronic rather than the acute effects of
repeated exposure to acroleln. Parameters examined were lung function
(Costa et al., 1986), animal weights, organ-to-body weight ratios, lung
composition and hlstologlcal changes 1n the lungs (Kutzman et al., 1985).
In rats exposed at 4.0 ppm, a substantial decrement In lung function was
observed. Expiratory flow rates were decreased and lung volumes were
enlarged, suggesting the presence of obstructive lesions 1n both small and
large airways. Rats exposed at 0.4 ppm acroleln showed "supernormal"
maximal air flows. Parenchymal tissue density of the lungs was found to be
significantly Increased (+15%) In this group, but was not affected at the
higher exposure concentrations. Costa et al. (1986) stated that the
Increase In air flow and tissue density at 0.4 ppm provided evidence of
parenchymal restriction. The authors concluded that under the exposure
conditions used In the study, acroleln produced contradictory functional
lesions at the 4.0 ppm and 0.4 ppm exposure levels. These effects were
essentially cancelled In the 1.4 ppm exposed group.
Other effects of acroleln exposure were reported by Kutzman et al.
(1985). At 4.0 ppm, 32/57 male rats died while none of the 8 exposed
females died. The average weights of the 4.0 ppm exposed rats were signifi-
cantly less than controls, while weights of the 1.4 and 0.4 ppm exposed rats
did not differ from controls. Organ-to-body weight ratios were measured In
8 male rats from each exposure group. The ratios of all organs except the
liver and spleen were significantly greater (p<0.05) In the 4.0 ppm rats
than \r\ the other groups. The greatest Increase was observed 1n the
lung-to-body weight ratio.
0103h -8- 10/23/86
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, Cellular contents of lungs from male rats exposed to 4.0 ppm acroleln
varied from control values; DNA was 117% of the control value, protein.
120%, elastln, 174% and collagen, 137%. Except for an Increase In collagen
In rats exposed at 1.4 ppm (113% of control value), the composition of the
lungs of rats exposed at 0.4 and 1.4 ppm were similar to controls.
H1stolog1cal examination of lungs from rats found dead or moribund that
were exposed at 4.0 ppm showed severe acute bronchopneumonla (Kutzman et
al., 1985). Focal alveolor edema with sloughed cells In the bronchi and
bronchioles was observed; many airways were plugged. Tracheal edema with
erosion of the mucosal epithelium was also observed 1n these rats. Lungs
from the 4.0 ppm acroleln-exposed survivors showed bronchlolar epithelial
necrosis and sloughing, bronchlolar mucopurulent plugs with macrophages and
focal pneumonltls; edema 1n the trachea and perlbronchlal lymph nodes was
also observed. Bronchlolar epithelial necrosis and sloughed cells 1n the
lumen were observed In 3 of the 31 1.4 ppm rats examined, as were Increased
numbers of alveolar macrophages and enhanced type II cell hyperplasla. No
pulmonary lesions attributable to acroleln were observed 1n the 0.4 ppm
exposure group.
Bouley et al. (1975, 1976) studied the effect of acroleln exposure on
the susceptibility of rats to Samonella enteritis. In this study, 110 SPF
OFA male rats were continuously exposed to acroleln vapor at 0.55 ppm (1.26
mg/m3) for up to 77 days. A control group of 110 rats was Included In the
study. After 60 days of exposure, the mean body weights of acroleln-exposed
rats were -80% of controls. Lung-to-body weight ratios were similar between
exposed and control rats sacrificed at 15 and 32 days, but were higher In
rats after 77 days of exposure.
0103h -9- 10/23/86
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' Rats challenged with an L05Q of airborne Salmonella enteritis showed a
significantly Increased susceptibility on day 18 but not on day 24. At day
18, 15/16 exposed rats died compared with 8/15 controls (p<0.05). After 63
days of exposure, death rates as a result of Salmonella Infection were
similar In both exposed and control rats (10/10), Indicating to the Investi-
gators that an adaptation phenomenon! had occurred after ~3 weeks of exposure.
3.2. CHRONIC
3.2.1. Oral. Data regarding the toxldty of chronic exposure to acroleln
are very limited. In an unpublished study, L1j1nsky (n.d.) gave acroleln to
rats In a limited amount of drinking water at 100, 250 or 625 ppm, 5 days/
week for up to 2 years. Mortality of the rats was not affected by acroleln
treatment; because carclnogenlclty was the only other endpolnt examined,
details of this study will be presented In Section 4.2.1.
3.2.2. Inhalation. The only chronic Inhalation study available was
conducted by Feron and Kruysse (1977), -who exposed 18 male and 18 female
Syrian golden hamsters to 4 ppm (9.2 mg/m3) acroleln for 7 hours/day, 5
days/week for 52 weeks. Similar groups of control hamsters were exposed to
filtered air. During the exposure period, hamsters were weighed monthly and
observed for toxic signs. After 52 weeks of exposure, 3 males and 3 females
were killed. The surviving hamsters were observed until week 81 when they
were sacrificed. Hematological and blood biochemical determinations were
conducted on all hamsters. At necropsy, organ weights were recorded and
organs were fixed for hlstopathologlcal examination.
Hamsters exposed to acoleln experienced . eye Irritation, excessive
salivation and nasal discharge during the first week of the study. As the
exposure continued, these signs were no longer observed. During the
exposure period, the average body weights of exposed males and females were
0103h -10- 10/23/86
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lower than those of the controls; these differences decreased during the
postexposure period. A statistically significant Increase In hemoglobin
content and packed cell volume was observed 1n acroleln-exposed females.
The remaining hematologlcal and blood biochemical parameters were not
affected.
The only statistically significant organ weight differences were found
In female hamsters; liver weights were slightly decreased and lung weights
were Increased. The only h1stopatho1og1cal changes attributable to acrolein
exposure were found 1n the nasal cavity, where a moderate degree of Inflam-
mation and epithelial metaplasia was observed. About 20% of the hamsters
killed at week 81 still showed effects of acrolein exposure 1n the nasal
cavity as Indicated by thickened mucosa and exudation 1n the lumen.
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. Pertinent data regarding the teratogenlc effects of
acrolein following oral exposure could not be located In the available
literature.
3.3.2. Inhalation. As part of a subchronlc Inhalation study, Bouley et
al. (1976) examined the reproduction of rats exposed to acrolein. Hale and
female SPF OFA rats were exposed continuously to 0.55 ppm {1.26 mg/m3)
acrolein vapor for 26 days. Mating was Initiated on the fourth day of
exposure and females were examined 22 days after Initiation of cohabitation.
No significant difference was noted 1n the number of pregnant rats, the
number of fetuses or the mean weights of the fetuses. No further data were
presented.
3.4. TOXICANT INTERACTIONS
Kane and Alarle (1978) studied the effects of simultaneous exposure to
formaldehyde and acrolein. Groups of four Swiss-Webster mice were exposed
0103h -11- 01/13/87
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ta varying concentrations of acroleln, formaldehyde alone or the two In
combination. Respiratory rates, which decrease with greater Irritation,
were measured as an Index of sensory Irritation. Eleven I0-m1nute exposures
were conducted In which the acroleln concentration ranged from 0.12-8.97 ppm
(0.28-20.6 mg/m3) and the formaldehyde concentration ranged from 0.33-9.73
ppm (0.41-11.95 mg/m3). Data from these exposures were used In a mathe-
matical model that describes the Interaction of agents acting at a single
sensory receptor site. From the results, Kane and AlaMe (1978) concluded
that acroleln and formaldehyde act 1n competitive antagonism for the same
receptor sites when causing sensory Irritation.
In a another study examining the Interaction of formaldehyde with
acroleln, Babluk et al. (1985) exposed male Fischer 344 rats to formaldehyde
at 15 ppm (18 mg/m3). 6 hours/day for 9 days, and then on the tenth day
challenged the rats with acroleln vapor. Sensory Irritation was determined
by measuring the respiratory rate depression during exposure. A depression
In respiratory rate Is a protective defense against respiratory Irritants; a
lower respiratory rate allows less chemical Into the lower respiratory tract.
The results of this study (Babluk et al., 1985) Indicated that 1n
nonpretreated rats, 6.0 ppm (13.8 mg/m3) acroleln was the RD«-n- I"
formaldehyde pretreated rats, 29.6 ppm (67.9 mg/m3) acroleln, a 5-fold
Increase, was required to reach the R05Q-
In a chronic Inhalation study, Feron and Kruysse (1977) examined the
effect of acroleln on the Cc'rdnogenlc potential of benzo(a)pyrene and
dlethylnltrosamlne. Hamsters exposed to acroleln vapor at 4 ppm (9 mg/m3)
for 52 weeks and to weekly In^.ratracheal Instillations of benzo(a)pyrene or
weekly Injections of d1ethylr»1trosam1ne did not show Increased tumor Inci-
dences. Acroleln did appear to shorten the t1me-to-tumor 1n the benzo(a)-
pyrene-dosed group.
0103h -12- 10/23/86
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4. CARCINOGENICITY
4.1. HUMAN DATA
Pertinent data regarding the carcinogenic potential of acroleln In
humans following oral or Inhalation exposure could not be located In the
available literature.
4.2. BIOASSAYS
4.2.1. Oral. The only animal study available concerning the carcinogenic
potency of acroleln by the oral route was an unpublished study by Lljlnsky
(n.d.). In this study, groups of 20 male Fisher 344 rats, caged In groups
of 4, were provided with 80 ml drinking water/cage, which contained
acroleln at 100, 250 or 625 ppm, 5 days/week for 120, 120 and 100 weeks,
respectively. On the remaining 2 days each week, rats were provided with
tap water ad. libitum, because 1n the previous 5 days access to drinking
water containing acroleln was limited to less than expected consumption to
Insure 1ngest1on of the full dose of acroleln. A group of 20 female rats
were treated In a similar manner with water containing 625 ppm acroleln.
Whether female rats were treated at the lower doses 1s unclear. The manner
of treatment of the control group of 20 male and 20 female rats was not
specified 1n the paper. At the end of the treatment period, rats were
allowed to die naturally, and survivors were sacrificed at 130 weeks. All
rats were necropsled and all major organs were examined hUtoToglcally.
The only significant result was an Increase 1n the Incidence of rare
adrenal cortex adenomas In female rats treated at 625 ppm (5/20 treated,
0/20 controls; p=0.02). At the NCI - Frederick Cancer Research Facility,
where this study was completed, the historical Incidence of this tumor was
12/263 (4.6X) 1n untreated or "solvenf'-treated females.
4.2.2. Inhalation. In the chronic Inhalation study conducted by Feron
and Kruysse (1977) (see Section 3.2.2.), no statistically significant
0103h -13- 03/23/87
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U.S. EPA. 1980b. Hazard Profile for Chloroethane. Prepared by the Office
of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Solid Waste, Washington,
DC.
U.S. EPA. 1980c. Guidelines and Methodology Used 1n the Preparation of
Health Effect Assessment Chapters of the Consent Decree Water CrHerl-a
Documents. Federal Register. 45(231): 49347-49357.
U.S. EPA. 1983. Methodology and Guidelines for Reportable Quantity Deter-
minations Based on Chronic Toxldty Data. Prepared by the Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office,
Cincinnati, OH for the Office of Solid Waste- and Emergency Response,
Washington, DC.
U.S. EPA. 1986a. Summary Review of Health Effects Associated with Mono-
chloroethane: Health Issue Assessment. Internal Review Draft. Prepared by
the Office of Health and Environmental Assessment, Environmental Criteria
and Assessment Office. Research Triangle Park, HC.
U.S. EPA. 1986b. Health and Environmental Effect Profile for Methyl
Chloride. Prepared by the Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH for the Office
of Solid Waste and Emergency Response, Washington, DC.
U.S. EPA. 1986c. Guidelines for Carcinogen Risk Assessment. Federal
Register. 51(185): 33992-34003.
0087h -14- 08/05/87
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dose-related response for acroleln In S^. typhlmurlum strain TA104, a new
strain designed to detect peroxides and other oxldants. Hales (1982)
reported that acroleln was nonmutagenlc In S^. typhlmurlum strain TA1535.
Haworth et al. (1983) found that acroleln was negative In £^ typhlmurlum
strains TA1535. TA1537, TA98 and TA100 with S-9 metabolic activation from
both rat and hamster livers.
Acroleln was not mutagenlc 1n Escherlchla coll strain K12/343/113
(Ellenberger and Mohn, 1977). Hemm1nk1 et al. (1980) reported acroleln to
be weakly mutagenlc In £_._ coll strain WP2 uvr A (trp~).
Acroleln has been tested for the Induction of sex-linked recessive
lethals In Drosophlla. In a study by Rapaport (1948), DrosophUa larvae
were allowed to feed on nutrient medium containing acroleln. The concentra-
tion of acroleln was not reported, but the level used was reported to cause
death In >75% of the treated larvae. The Incidence of sex-linked recessive
lethals In survivors of acroleln treatment was 2.23%, compared with 0.19% In
controls. When adult male Drosphlla were fed a 5X sucrose solution contain-
ing 3000 ppm acroleln or were Injected with acroleln at 200 ppm In saline,
however, the Incidence of recessive lethals In treated flies was essentially
Identical to controls (ZlmmeMng et al., 1985).
Au et al. (1980) tested acroleln for sister chromatld exchange and
chromosome breaks In Chinese hamster ovary cells. The results showed a
dose-related response for sister chromatld exchange without S-9, but were
negative with S-9 metabolic activation. Tests for chromosome breaks In
Chinese hamster ovary cells were confounded by toxldty, but the Investi-
gators concluded that the response was not a true Indication of the
mutagenlc effects of acroleln (Au et al., 1980).
0103h -15- 01/13/87
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Epstein et al. (1972) studied acroleln In a dominant lethal assay. Male
8- to 10-week-old ICR mice received single 1ntraper1toneal Injections of 1.5
or 2.2 mg/kg acroleln and were mated with three untreated females/week for 8
weeks. The authors stated that the Incidence of early fetal deaths and
prelmplantatlon losses were within control limits.
4.4. ' HEIGHT OF EVIDENCE
The Increased Incidence of adrenal cortex adenomas In female rats
treated at 625 ppm In drinking water provides limited evidence that acroleln
may be carcinogenic to animals. Results of mutagenldty tests are equi-
vocal; In some tests acroleln has not been mutagenlc, while 1n other tests
1t has been shown to be weakly mutagenlc. Structural activity relationships
also suggest possible carcinogenic activity of acroleln.
There are no ep1dem1olog1cal studies relating acroleln exposure to car-
dnogenlclty In the present data base. The skin painting and subcutaneous
studies of acroleln are Inadequate to assess carcinogenic potential; similar
studies of Its metabolite glycldaldehyde are, however, supportive of a car-
cinogenic potential. There are two different families of chemical compounds
that may be functionally related to acroleln: aldehydes and dlenes. The
first group Include chemicals such as formaldehyde and acetaldehyde, which
are considered to be probable human carcinogens by the U.S. EPA. The second
group Includes dlene-vlnyl compounds such as ethylene oxide, acrylonltrlle,
vinyl chloride and 1,3-butadlene. These have been classified as probable or
known (vinyl chloride) human carcinogens.
Based upon 1) the structural relationship between acroleln and related
compounds that are potentially carcinogenic to humans, 2) animal studies
that suggest a carcinogenic potential for a known metabolite of acroleln,
and 3) the lack of ep1dem1olog1cal data, acroleln 1s considered to have
0103h -16- 03/11/87
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"limited" animal evidence for carclnogenlclty (U.S. EPA, 1986a). Because
the evidence In animals 1s limited, acroleln should be classified 1n IARC
Group 3; that 1s, 1t cannot be classified as to Its carclnogenlclty.
According to the U.S. EPA classification scheme (U.S. EPA, 1986b), acroleln
may be classified In Group C, limited animal evidence of carclnogenlclty.
0103h -17- 08/03/87
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5. REGULATORY STANDARDS AND CRITERIA
In developing an ambient water quality criteria for acroleln, the U.S.
EPA (1980a) derived an RfD of 1.56xlO~2 mg/kg/day, or 1.09 mg/day for a 70
kg human. This RfD was derived from the study by Newell (1958), In which no
effects were observed In rats provided with drinking water containing
acroleln at 200 mg/t for 90 days. A rat body weight of 450 g, a water
consumption of 35 ml/day and an uncertainty factor of 1000 were used to
calculate this RfD (U.S. EPA, 1980a). Assuming a 70 kg human drinks 2 i
of water/day and eats 6.5 g of fish/day with a bloconcentratlon factor of
215, a water quality criteria for acroleln of 0.32 mg/l was derived from
the RfD of 1.56xlO~* mg/kg/day (U.S. EPA, 1980a).
The RfD of 1.56xlO~a mg/kg/day was also presented In U.S. EPA (1985a),
and rounded to 1.6xlO~a mg/kg/day In U.S. EPA (1985a).
The ACGIH (1986) TLV-THA for acroleln 1s 0.1 ppm (-0.25 mg/m3); the
TLV-STEL 1s 0.3 ppm (-6.8 mg/m3). ACGIH (1986) stated that the TWA-TLV
Is sufficiently low to minimize but not to prevent Irritation to all exposed
Individuals. The OSHA (1985) PEL Is also 0.1 ppm.
0103h -18- 08/03/87
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6. RISK ASSESSMENT
6.1. SUBCHRONIC REFERENCE DOSE (RfD$)
6.1.1. Oral (RfDgJ. The unpublished study by Lljlnsky (n.d.) showed
an Increased Incidence of adrenal cortex adenomas 1n female rats provided
with acroleln 1n their drinking water. Since a q * was not calculated at
this time because of Inadequate data, but concern over the carclnogenlclty
of acroleln exists, an RfDSQ value will not be derived.
6.1.2. Inhalation (RfDSI). Limited evidence Indicates that acroleln Is
an oral carcinogen; therefore, an RfOSI value will not be derived.
6.2. REFERENCE DOSE (RfD)
6.2.1. Oral (RfDQ). Because the above stated concerns also apply to an
RfD, an RfDQ value will not be calculated for acroleln.
6.2.2. Inhalation (RfD.). Limited evidence Indicates that acroleln Is
an oral carcinogen; therefore, an RfD, value will not be derived.
6.3. CARCINOGENIC POTENCY (q^)
6.3.1. Oral. The study by Lljlnsky (n.d.) provides limited evidence that
acroleln may be carcinogenic following oral exposure. In this study, an
Increase 1n the Incidence of adrenal cortex adenomas was observed Vn treated
female rats (5/20 treated, 0/20 control). The treated females, four rats/
cage, were provided with 80 ml drinking water/cage/day which contained 625
ppm acroleln, 5 days/week for 100 weeks. The remaining 2 days/week, the
rats were provided with tap water ad libitum. The rats were allowed to die
naturally, with survivors sacrificed at 130 weeks. The treatment of the
control group of 20 female rats, particularly with regard to limited access
to drinking water, was not specified.
0103h -19- 08/03/87
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The Increased Incidence of adrenal cortical adenomas In treated female
rats cannot be used to derive a q * for oral exposure. Adenomas without
other "tumor" Incidences are considered to be Inadequate data for q *
derivation.
6.3.2. Inhalation. The only chronic Inhalation study of acroleln (Feron
and Kruysse, 1977) did not show an Inceased tumor Incidence; therefore, an
Inhalation q * cannot be calculated.
0103h -20- 08/03/87
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7. REFERENCES
ACIGH (American Conference of Governmental Industrial Hyglenlsts). 1986.
Documentation of Threshold Limit Values and Biological Exposure Indldes,
5th ed. Cincinnati, OH. p. 11.
Albln, T.B. 1962. Handling and toxicology. .In: Acroleln, C.W. Smith, Ed.
John Wiley and Sons, Inc., New York. p. 234. (Cited In U.S. EPA, 1980a)
Au, W., O.Z. Sokova, B. Kopln and F.E. Arrlghl. 1980. Cytogenlc toxlclty
of cyclophosphamlde and Us metabolites jjn vitro. Cytogenet. Cell Genet.
26: 108-116.
Babluk, C., U.H. Stelnhagen and C.S. Barrow. 1985. Sensory Irritation
response to Inhaled aldehydes after formaldehyde pretreatment. Toxlcol.
Appl. Pharmacol. 79(1): 143-149.
Beauchamp, R.D., Jr., D.A. Andjelkovlch, A.D. Kllgerman, K.T. Morgan, H.D.
Heck. 1985. A critical review of the literature on acroleln toxlclty. CRC
Crlt. Rev. Toxlcol. 14(4): 309-380.
Bouley, G., A. Oubreull, J. Godln and C. Boudene. 1975. Effects of a small
dose of acroleln constantly Inhaled by rats. Eur. J. Toxlcol. Environ. Hyg.
8: 291-297. (Cited 1n U.S. EPA, 1986a)
Bouley. G., A. Oubreull, J. Godln, M. Bolsset and C. Boudene. 1976.
Phenomena of adaption In rats continuously exposed to low concentration of
acroleln. Ann. Occup. Hyg. 19(1): 27-32.
0103h -21- 08/03/87
-------
Brabec, M.J. 1982. Aldehydes and acelates. in: Patty's Industrial Hygiene
and Toxicology, Vol. 2A, 3rd ed., G.D. Clayton and R.E. Clayton, Ed. John
Wiley and Sons, Inc., New York. p. 2266, 2634-2637, 2648-2656.
Carson, B.L., C.M. Beall, H.V. Ellis, L.H. Baker and B.L. Herndon. 1981.
Acroleln Health Effects. EPA 460/3-81-034. NTIS PB82-161282.
Costa, D.L., R.S. Kutzman, J.R. Lehmann and R.T. Drew. 1986. Altered lung
function and structure In the rat after subchronlc exposure to acroleln.
Am. Rev. Resplr. D1s. 133(2): 286-291.
Oramlnskl, U., E. Eder and D. Henschler. 1983. A new pathway of acroleln
metabolism 1n rats. Arch. Toxlcol. 52: 243.
Egle, J.L., Jr. 1972. Retention of Inhaled formaldehyde, proplonaldehye,
and acroleln 1n the dog. Arch. Environ. Health. 25: 119-124.
Ellenberger, J. and G.R. Mohn. 1977. Mutagenlc activity of major mammalian
metabolites of cyclophosphamlde toward several genes of Escherlchla cojl.
J. Toxlcol. Environ. Health. 3: 637-650. (Cited In U.S. EPA, 1986a)
Epstein, S.S., E. Arnold, J. Andrea, W. Bass and Y. Bishop. 1972. Detec-
tion of chemical mutagens by dominant lethal assay In the mouse. Toxlcol.
Appl. Pharmacol. 23: 288-325.
Feron, V.J. and A. Kruysse. 1977. Effects of exposure to acroleln vapor In
hamsters simultaneously treated with benzo(a)pyrene or dlethylnltrosamlne.
J. Toxlcol. Environ. Health. 3: 379-394.
0103h -22- 08/03/87
-------
Feron, V.J., A. Kruyssee, H.P. Til and H.R. Immel. 1978. Repeated exposure
' »
to acroleln vapor. Subacute studies In hamsters, rats and rabbits.
Toxicology. 9: 47-57.
Hales, B. 1982. Comparison of the mutagenldty and teratogenldty of
cyclophosphamlde and Its active metabolites, 4-hydroxycyclophosphamlde,
phosphoramlde mustard, and acroleln. Cancer. Res. 42: 3016-3021.
Hansch, C. and A.J. Leo. 1985. Medchem Project. Pomona College,
Claremont, CA.
Haworth, S., T. Low!or, K. Mortelmans, W. Speck and E. Zelger. 1983.
Salmonella mutagenldty test results for 250 chemicals. Environ. Hutagen.
1: 3-142.
Hemmlnkl, K., K. Falck and H. Va1n1o. 1980. Comparison of alkylatlng rates
and mutagenldty of direct acting Industrial and laboratory chemicals.
Arch. Toxlcol. 46: 277-285.
Kane, I.E. and Y. Alarle. 1978. Evaluation of sensory Irritation from
acroleln-formaldehyde mixtures. Am. Ind. Hyg. Assoc. J. 39: 270-274.
(Cited In U.S. EPA, 1986a)
Kutzman, R.S., E.A. Popenoe, M. Schmaeler and R.T. Drew. 1985. Changes In
rat lung structure and composition as a result of subchronlc exposure to
acroleln. Toxicology. 34(2): 139-151.
0103h -23- 08/03/87
-------
LlJInsky, W. n.d. Chronic studies In rodents of vinyl acetate and
compounds related to acroleln. Unpublished. NCI-Freder1ck Cancer Research
Facility, Frederick, MD.
LlJInsky, W. and A.M. Andrews. 1980. Mutagenldty of vinyl compounds In
Salmonella typhlmurlum. Teratogen. Carcinogen. Mutagen. 1: 259-267.
Lutz, 0., E. Eder, T. Neudecker and 0. Henschler. 1982. Structure-
mutagenldty relationships 1n 2,8-unsaturated carbonyllc compounds and their
corresponding allyllc alcohols. Mutat. Res. 93: 303-315.
Lyon, J.P., L.J. 'Jenrlng, Jr., R.A. Jones, R.A. Coon and J. Slegel. 1970.
Repeated and continuous exposure of laboratory animals to acroleln.
Toxlcol. Appl. Pharmacol. 17: 726-736.
Marnett, L.J., H.K. Hurd, M.C. Hollsteln, D.E. Levin, H. Esterbaure and 8.N.
Ames. 1985. Naturally occurring carbonyl compounds are mutagenlc In
Salmonella tester strain TA104. Mutat. Res. 148: 25-34. (Cited In U.S.
EPA. 1986a)
NAS (National Acacemy of Sciences). 1977. Drinking Water and Human Health.
Washington, DC.
Newell, G.W. 19118. Acute and Subacute Toxldty of Acroleln. Stanford
Research Institute. SRI Project No. 5-868-2. (Cited In NAS, 1977)
0103h -24- 08/03/87
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OSHA (Occupational Safety and Health Administration). 1985. Safety and
Health Standards. Code of Federal Regulations. 29: 1910.1000.
Rapaport. I.A. 1948. Mutations Induced by unsaturated aldehydes. Ookl.
Akad. Nauk. USSR 61: 713-715. (Rus.) (Cited In U.S. EPA, 1986a)
Salamon, M.H. and F.J. C. Roe. 1956. Further tests for tumor Initiating
activity: N, N-01-(2 chloroethyl)-p-am1nopheny1-butyr1c acid (CB 1348) as an
Initiator of skin tumor formation In the mouse. Br. J. Cancer. 10:
363-378. (Cited In U.S. EPA, 1986a)
Stelner, P.E., R. Steele and F.C. Koch. 1943. The possible cardnogenlcHy
of overcooked meats, heated cholesteral, acroleln and heated sesame oil.
Cancer Res. 3: 100-107. (Cited 1n U.S. EPA, 1986a)
U.S. EPA. 1980a. Ambient Water Quality Criteria Document for Acroleln.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Hater Regu-
lations and Standards, Washington, DC. EPA 440/5-80-016. NTIS PB81-117277.
U.S. EPA. 1980b. Guidelines and Methodology Used 1n the Preparation of
Health Effect Assessment Chapters of the Consent Decree Water Criteria
Documents. Federal Register. 45(231): 49347-49357.
0103h -25- 08/03/87
M.S.
Region 5, Library (PI-12J)
77 West jacteon Boulevard, 12th
t 60604-3590
-------
, ,U.S. EPA. 1983. Methodology and Guidelines for Reportable Quantity Deter-
minations Based on Chronic Tox1c1ty Data. Prepared by the Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office,
Cincinnati, OH for the Office of Solid Waste and Emergency Response,
Washington, DC.
U.S. EPA. 1985a. Health and Environmental Effects Profile for Acroleln.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Waste
and Emergency Response, Washington, DC.
U.S. EPA. 1985b. Reference Values for Risk Assessment. Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OK for the Office of Solid Waste, Washington,
DC.
U.S. EPA. 1986a. Health Assessment Document for Acroleln. Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Research Triangle Park, NC for the Office of A1r Quality
Planning and Standards. Washington, OC. EPA 600/8-86-014A.
U.S. EPA. 1986b. Guidelines for Carcinogen Risk Assessment. Federal
Register. 51(185): 33992-34003.
ZlmmeMng, S., J.H. Mason, R. Valencia and R.C. Woodruff. 1985. Chemical
mutagenesls testing In DrosophHa. II. Results of 20 coded compounds tested
for the National Toxicology Program. Environ. Mutagen. 7(1): 87-100.
0103h -25- 08/06/87
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EPA/600/8-88/013
July, 1987
HEALTH EFFECTS ASSESSMENT
FOR ACROLEIN
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
CINCINNATI, OH 45268
-------
-------
TECHNICAL RETORT DATA
(Htmt nud liutntctmiu on Ou revtnt be fort eomplttingl
EPA/600/8-88/013
3. RECIPIENT'S ACCESSION NO.
PB88-179494
4. TITLE AND SUBTITLE
Health Effects Assessment for Acrolein
S. REPORT DATE
•. PERFORMING ORGANIZATION CODE
7. AUTMOR(S)
•. PERFORMING ORGANIZATION REPORT NO
9. PERFORMING ORGANIZATION NAME AND AOORESS
10. PROGRAM ELEMENT NO.
11. CONTRACT/CHANT NO.
12. SPONSORING AGENCY NAME AND AOORESS
13. TYPE OF REPORT AND PERIOD COVERED
Environmental Criteria and Assessment Office
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati. QH 45268
14. SPONSORING AGENCY CODE
EPA/600/22
15. SUPPLEMENTARY NOTES
16. ABSTRACT
This report summarizes and evaluates information relevant to a preliminary interim
assessment of adverse health effects associated with specific chemicals or compounds.
The Office of Emergency and Remedial Response (Superfund) uses these documents in
preparing cost-benefit analyses under Executive Order 12991 for decision-making under
CERCLA. All estimates of acceptable intakes and carcinogenic potency presented in
this document should be considered as preliminary and reflect limited resources
allocated to this project. The intent in these assessments is to suggest acceptable
exposure levels whenever sufficient data are available. The interim values presented
reflect the relative degree of hazard associated with exposure or risk to the
chemical(s) addressed. Whenever possible, two categories of values have been
estimated for systemic toxicants (toxicants for which cancer is not the endpoint of
concern). The first, RfD$ or subchronic reference dose, is an estimate of an exposure
level that would not be expected to cause adverse effects when exposure occurs during
a limited time interval. The RfD is an estimate of an exposure level that would not
be expected to cause adverse effects when exposure occurs for a significant portion
of the lifespan. For compounds for which there is sufficient evidence of
carcinogenicity, qi*s have been computed, if appropriate, based on oral and
inhalation data if available.
17.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b. IDENTIFIERS/OPEN ENDED TERMS C. COS AT I Field/Group
1«. DISTRIBUTION STATEMENT
Public
19. SECURITY CLASS (This Report!
Unclassified
21. NO. OF PAGES
20. SECURITY CLASS
Unclassified
22. PRICE
EPA Pw» 2220.1 (»•». 4-77) pRKvious COITION i> OMOLKTK
U.S. Environmental Protection Agemry
Region 5, Library (PL-12J)
ft*? #ck^§?ule*>«i. 12th Floor
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